Purpose - We investigated whether cardiac rehabilitation participation increases circulating endothelial progenitor cells (EPCs) and benefits vasculature in patients already on stable therapy previously shown to augment EPCs and improve endothelial function. [unreadable] Methods - Forty-six of 50 patients completed a 36-session cardiac rehabilitation program: 45 were treated with HMG-CoA redctase inhibitor (statin) therapy 1 month (average baseline LDL-C 81 mg/dL). Mononuclear cells isolated from blood were quantified for EPCs by flow cytometry (CD133+/VEGFR-2+ cells) and assayed in culture for EPC colony-forming units (CFUs). In 23 patients, EPCs were stained for annexin-V as a marker of apoptosis and nitrite was measured in blood as an indicator of intravascular nitric oxide (NO). [unreadable] Results - EPCs increased from 355 to 6310 cells/mL, and EPC-CFUs increased from 0.90.2 to 3.10.6 per well (both P<0.01), but 11 patients had no increase in either measure. Those patients whose EPCs increased from baseline showed significant increases in nitrite and reduction in annexin-V staining (both P<0.01), versus no change in patients without increase in EPCs. Over the course of the program, EPCs increased prior to increase in nitrite in blood. [unreadable] Conclusions - Cardiac rehabilitation by CAD patients on stable statin therapy and with LDL-C at goal increases EPC number, EPC survival and endothelial differentiation potential, associated with increased NO in blood. Although this response was observed in most patients in our study, a significant minority showed neither EPC mobilization nor increased NO in blood.